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Step I Beta2 antagonist increase insulin release?
Started by TripleB
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I would think that for the cortisol thing they didn't want people thinking that cortisol directly stimulates insulin release.
Where? I remember reading beta 2 function is insulin release in the pharm chapter! How can the opposite be mentioned in the same book? Which chapter did you see it?
Beta-2 agonism increases insulin release.
In contrast, alpha-2 agonism decreases insulin release.
This is high-yield and I had seen this in several practice questions.
In contrast, alpha-2 agonism decreases insulin release.
This is high-yield and I had seen this in several practice questions.
This conforms to what I have read as well. OP's post is a little confusing though.
+1 to phloston and oldstylenanny.
when in doubt, first aid is wrong
when in doubt, first aid is wrong
Yeah this is what is says in FA 2013. I'm not quite sure what the OP is talking about...maybe it was something corrected in the FA 2012 errata.
Actually I'm fairly certain I read it as mentioned above in the Pharmacology chapter in FA2012, which was why I was asking the OP which chapter of the same book he/she got the posted contradictory info from.
Ok, let me clarify: on page 315 on FA 2012, it says "hyperglycemia, GH, and cortisol increase insulin...b-agonists stimulate insulin release" which makes sense to me. In the errata of FA 2012, they changed the text to "Replace the paragraph about Regulation with this: Hyperglycemia, GH, and β2- antagonists increase insulin. Hypoglycemia, somatostatin, and α2-agonists decrease insulin." This is also what is on FA 2013 pg 288.
So I am wondering what caused them to do this.
The most high yeild connection between beta-2 antagonists and the pancreas/insulin is probably that:
Non-specific (B1/B2) Antagonists, like propranolol, should not be used in diabetic patients, as they mask the early adrenergic side effects of HYPOglycemia. Hypoglycemia triggers catechols which cause tachycardia, diaphoresis, anxiety, etc. early on. This can be very dangerous in these patients, if these symptoms are masked.
This seems like the most logical clinical scenario that would come up on the boards. I just can't see them asking flat out, "Do Beta-antagonists increase or decrease insulin release in the pancreas?" Try and think of "how" they would ask the question. Figure out "why" its important clinically.
And, another thing. Remeber that although Beta-2 adrenergic Agonists can cause insulin release from the pancreas, they also stimulate Glycogenolysis in the liver, which can lead to hyperglycemia. At least, this is what i can remember on the subject. I think these would be more of the systemic Beta-2 agonists, like PO Albuterol and Clenbuterol and not the aerosolized kind used in acute asthma management. Typically not going to see hyperglycemia in an asthmatic, unless they are on PO steroids or they just took 15 puffs of their inhaler.
Non-specific (B1/B2) Antagonists, like propranolol, should not be used in diabetic patients, as they mask the early adrenergic side effects of HYPOglycemia. Hypoglycemia triggers catechols which cause tachycardia, diaphoresis, anxiety, etc. early on. This can be very dangerous in these patients, if these symptoms are masked.
This seems like the most logical clinical scenario that would come up on the boards. I just can't see them asking flat out, "Do Beta-antagonists increase or decrease insulin release in the pancreas?" Try and think of "how" they would ask the question. Figure out "why" its important clinically.
And, another thing. Remeber that although Beta-2 adrenergic Agonists can cause insulin release from the pancreas, they also stimulate Glycogenolysis in the liver, which can lead to hyperglycemia. At least, this is what i can remember on the subject. I think these would be more of the systemic Beta-2 agonists, like PO Albuterol and Clenbuterol and not the aerosolized kind used in acute asthma management. Typically not going to see hyperglycemia in an asthmatic, unless they are on PO steroids or they just took 15 puffs of their inhaler.
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